P K Pang

University of Alberta, Edmonton, Alberta, Canada

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Publications (247)721.54 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Alcoholic extracts of the roots and leaves of three Echinacea species (E. purpurea, E. angustifolia and E. pallida) were analysed for the presence of characteristic chemicals by HPLC directly coupled to ultraviolet absorbance and electrospray mass spectrometric detectors. The method permitted rapid characterization and tentative identification of a large number of caffeoyl conjugates and alkamides in all the samples investigated. The roots of the three species differed markedly in their contents of characteristic compounds. Cichoric acid and verbascoside predominated in extracts of E. purpurea root whereas cynarine and dodeca-2E,4E,8Z,10Z/E-tetraenoic acid isobutylamide were the major chemicals characteristic of E. angustifolia root extracts. Echinacoside and 6-O-caffeoylechinacoside predominated in extracts of E. pallida roots. Characteristic alkamides were also examined by electrospray tandem mass spectrometry (MS/MS) and these compounds provided characteristic fragmentation patterns. Extracts of the roots and leaves of all three species were found to have antioxidant properties in a free radical scavenging assay and in a lipid peroxidation assay.
    Journal of Pharmacy and Pharmacology. 02/2010; 53(6):849 - 857.
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    ABSTRACT: The effect of an indole-alkaloid mitragynine isolated from the Thai medicinal herb kratom (Mitragyna speciosa) on neurogenic contraction of smooth muscle was studied in guinea-pig vas deferens. Mitragynine inhibited the contraction of the vas deferens produced by electrical transmural stimulation. On the other hand, mitragynine failed to affect the responses to norepinephrine and ATP. Mitragynine did not reduce KCl-induced contraction in the presence of tetrodotoxin, prazosin and alpha,beta-methylene ATP. Mitragynine inhibited nicotine- or tyramine-induced contraction. By using the patch-clamp technique, mitragynine was found to block T- and L-type Ca2+ channel currents in N1E-115 neuroblastoma cells. In the Ca2+ measurement by a fluorescent dye method, mitragynine reduced KCl-induced Ca2+ influx in neuroblastoma cells. The present results suggest that mitragynine inhibits the vas deferens contraction elicited by nerve stimulation, probably through its blockade of neuronal Ca2+ channels.
    Life Sciences 12/2005; 78(2):187-94. · 2.56 Impact Factor
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    Fang Ba, Peter K T Pang, Christina G Benishin
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    ABSTRACT: Physiologically relevant concentrations of 17beta-estradiol (E2) are neuroprotective in both beta-amyloid protein 25-35 (Abeta) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced cytotoxicity in SK-N-SH cells. MPTP, but not Abeta, induces apoptosis in this cell line. The L-type calcium channel blocker nifedipine or decreased extracellular Ca(2+) concentration blocked Abeta-induced cell death, but not MPTP-induced cell death. Other blockers selective for different Ca(2+) channel subtypes had no effects on either Abeta or MPTP induced death. Western blot analysis for L-type Ca(2+) channel alpha(1)-subunits demonstrated that Abeta increases the expression of the neuronal alpha(1C) and alpha(1D) subunits of L-type channels. Both E2 and nifedipine inhibit the increase in expression of these by Abeta. MPTP also increases expression of alpha(1C) and alpha(1D), but the increases were not influenced by E2 or nifedipine. These observations suggested that Abeta cytotoxicity in SK-N-SH cells may involve increased availability of calcium to cells, whereas MPTP induced cytotoxicity does not require extracellular Ca(2+). Both cytotoxic models were associated with increased expression of Ca(2+) channel alpha(1) subunits, and neuroprotection associated with inhibition of that increase. These studies reveal that nifedipine, in addition to its direct action of nifedipine on Ca(2+) channels, may also protect neurons from Abeta toxicity through the suppression of the channel protein overexpression. A new action of dihydropyridines (DHPs) may be considered in the regulation of calcium homeostasis.
    Neurochemistry International 08/2004; 45(1):31-8. · 2.66 Impact Factor
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    ABSTRACT: Estrogen has been considered to be a neuroprotectant and a neuromodulator in many neuronal cell lines and tissue preparations. The protective effects of estrogen may be mediated through classical estrogen receptors (ERs), or may be due to its anti-oxidant properties which are independent of receptors. The current studies show that 17beta-estradiol (E2) is neuroprotective against beta-amyloid protein 25-35 (Abeta)-, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-, high density culture condition-, and serum deprivation-induced neuronal death in SK-N-SH human neuroblastoma cells. SK-N-SH cells express ERbeta, but not ERalpha, as detected by Western blot analysis. Among all the insults, MPTP, high density culture and serum deprivation induce apoptotic cell death in this cell system as detected by ELISA determination of mono/oligonucleosomes and DNA laddering, while Abeta induces necrotic cell death. The protective effects of E2 are abolished by the addition of tamoxifen and ICI 182,780 in the MPTP treated cells, but not in the other models, suggesting that the effect of E2 in the MPTP model is probably associated with activation of ERbeta. The addition of ICI 182,780 shows a mitogenic effect in SK-N-SH cells in the presence of E2 in control culture or in the Abeta treated groups. Also, ICI 182,780 induced expression of ERalpha. Collectively, the current studies suggest that E2 is neuroprotective in apoptotic and necrotic death induced by multiple insults in SK-N-SH human neuroblastoma cells. Involvement of ER is insult type dependent. ICI 182,780 is able to influence the expression of ERs, probably through upregulation of ERalpha when ERbeta is totally antagonized.
    Neurochemistry International 06/2004; 44(6):401-11. · 2.66 Impact Factor
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    ABSTRACT: Under basal conditions there is no observable nitric oxide synthase (NOS) activity in vascular smooth muscle (VSM). Pretreatment of endothelium-denuded aortic rings from Sprague-Dawley rats with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), (0.1 micromol/L) significantly attenuated phenylephrine (PE)-induced contractile responses in a dose-dependent manner. In the presence of 10 micromol/L Nomega-nitro-L-arginine (L-NNA) or 0.1 mmol/L aminoguanidine (AG), the inhibition of contractions at 10 nmol/L PE by H-7 was blocked by 88% or 52%, respectively. The blockade by antagonists was completely reversed by l-arginine but not by d-arginine, and alone they did not significantly alter PE-induced contraction of endothelium-denuded aorta. Methylene blue (MB, 50 micromol/L) also inhibited the action of H-7. The inhibitory effect of H-7 occurred after 5 minutes and was reversible. PE-induced contraction was also inhibited by the selective protein kinase C inhibitors calphostin C (10 micromol/L), and bisindolylmaleimide IV (Bis-IV, 10 micromol/L), but not by the selective protein kinase A inhibitor H-89 (0.1 micromol/L). These results indicate protein kinase C inhibits NOS activity in VSM under basal conditions. Incubation of tissues with either H-7 or calphostin C stimulates NO production, and immunocytochemical studies reveal the presence of NOS in VSM under basal conditions.
    Journal of Cardiovascular Pharmacology 03/2004; 43(2):281-7. · 2.38 Impact Factor
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    Fang Ba, Peter K T Pang, Christina G Benishin
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    ABSTRACT: A reliable in vitro cytotoxic system is essential in neurocytotoxic and neuroprotective research. The present study examined four cytotoxic insults with the SK-N-SH human neuroblastoma cell line. These were beta-amyloid protein (Abeta), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), high density culture, and serum deprivation induced neuronal death. These insults induced significant reduction in cell numbers after 96 h culture, in a concentration dependent manner. Among all the insults, MPTP, serum deprivation, and high density culture induced apoptosis after 96 h, while Abeta presumably induced necrotic neuronal death since apoptosis was not detectable. The p38 MAP kinase inhibitor, SB203580 (1 microM), and the PKC inhibitor, chelerythrine (5 microM) successfully inhibited the loss in viability caused by Abeta and the high density culture, respectively. Other kinase inhibitors, including the non-specific protein kinase inhibitor, H7, the PKA inhibitor 14-22 Amide, the PKG inhibitor, KT5823, and the protein tyrosine kinase inhibitor, AG18 had no effect on any of the four cytotoxic models. This system allows the study of neuroprotection under conditions where the different pathways and mechanisms of the neurons can be considered within one cellular system, removing variations which may be due to different cell type studied. The present studies describe an effective model system for screening potential neuroprotective agents.
    Journal of Neuroscience Methods 03/2003; 123(1):11-22. · 2.11 Impact Factor
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    ABSTRACT: Progesterone induced rapid relaxation of KCl-contracted tail artery helical strips from rats. The effect was dose dependent, with an IC50 (inhibitory concentration which produces 50% of the maximal response) of 8.9 microM progesterone. The actions of progesterone were not blocked by bicuculline, indicating that in this tissue the non-genomic actions of progesterone were not mediated via a gamma-aminobutyric acid (GABA)-A receptor. Fura-2 was used to measure intracellular calcium levels ([Ca(2+)](i)) in isolated vascular smooth muscle cells (VSMC). Incubation of cultured VSMC for 15 min with progesterone (10 microM) resulted in an inhibition of the KCl-induced [Ca(2+)](i )increase. The whole-cell patch-clamp technique was used to examine Ca(2+)-channel currents in the membrane of isolated VSMC. Progesterone suppressed the L-type Ca(2+)-channel currents in cells held at a potential of -40 mV. The effects of progesterone were quickly reversed by washout in all three experimental protocols suggesting that these effects on vascular tissues are non-genomic. The correlation of the effects on all these preparations, their time course and reversibility suggested that the rapid relaxation of the rat tail artery induced by progesterone is mediated at least in part by inhibition of L-type calcium channels, leading to inhibition of calcium responses in the VSMC of this tissue.
    Journal of Pharmacy and Pharmacology 01/2003; 54(12):1667-74. · 2.03 Impact Factor
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    ABSTRACT: Progesterone induced rapid relaxation of KCl-induced contraction of rat aortic rings. The relaxant effect of progesterone on aortic rings was concentration-dependent (over the range of 10(-10) to 10(-5) M) and partially dependent on the endothelium. Application of a nitric oxide (NO) synthase antagonist N(G)-monomethyl-L-arginine (L-NMMA, 10(-5) M) after progesterone treatment partially inhibited the relaxant effects of progesterone. This suggested that part of the effect was through the production of nitric oxide. Washing out the steroid hormone in the bath solutions could quickly reverse the inhibitory effects of progesterone on phasic tension generation in aortic rings. Five minutes after washout, the tension generation in aortic rings was completely restored. Cultured endothelial cells from rat aorta increased release of NO into culture media in response to a 60-min exposure to progesterone. Aldosterone and dexamethasone were also tested, and failed to relax KCl-induced contraction of aortic rings. These data suggest that the vascular effects of progesterone are not mediated by a genomic action of this steroid, and that the vascular effects are mediated partially through endothelial NO production.
    Journal of Pharmacy and Pharmacology 12/2002; 54(11):1529-34. · 2.03 Impact Factor
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    ABSTRACT: 1. There has been increasing awareness and use of natural preparations for health purposes by consumers. 2. However, recent studies have repeatedly shown that many natural products marketed as nutraceuticals or health food do not deliver the health benefit as claimed and are inconsistent from batch to batch. 3. The present paper describes the scientific rationale of such inconsistency and uses an antihypertensive preparation as an example to demonstrate the significant value of natural products if developed scientifically and properly.
    Clinical and Experimental Pharmacology and Physiology 09/2002; 29(8):731-4. · 2.41 Impact Factor
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    ABSTRACT: The aim of this study is to investigate the effects of Panax quinquefolius L. extract (PQE), Ginkgo biloba extract (GBE), and Hypericum perforatum extract (HPE), in combination or alone, on the survival and regeneration of axotomized retinal ganglion cells (RGCs) in an optic nerve transection model in adult hamsters. Unilateral transection of the optic nerve was performed to evaluate the effects of herbal extracts on the survival of axotomized RGCs. Effects of the herbal extracts on axonal regeneration of axotomized RGCs, on the other hand, were studied by attaching a peripheral nerve graft onto the transected ocular stump to induce regeneration. Operated animals received daily oral administration of vehicle or herbal extracts (PQE, GBE, and HPE), alone or in combination, for 7 and 21 days, respectively, in the survival and regeneration experiments. Surviving and regenerating RGCs were retrogradely labeled with Fluoro-Gold. The eyes were then enucleated and the retinas were flat-mounted for the counting of the labeled RGCs. Treatment with PQE, GBE and HPE alone failed to offer neuroprotection to injured RGCs. However, treatment with Menta-FX, a mixture of PQE, GBE, and HPE, significantly augmented RGC survival 7 days postaxotomy. Treatment with Menta-FX also induced a significant (87%) increase in the number of regenerating RGCs 21 days after optic nerve transection. This study demonstrates that herbs can act as a potential neuroprotective agent for damaged RGCs. It also suggests that the therapeutic value of herbal remedies can be maximized by the use of mixtures of appropriate herbs.
    Journal of Neurotrauma 04/2002; 19(3):369-78. · 4.30 Impact Factor
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    ABSTRACT: The effects of rat parathyroid hormone-related protein (rPTHrP) and bovine and rat parathyroid hormone (bPTH and rPTH) on L-type Ca2+ channels in UMR 106 cells were investigated using the patch clamp technique. rPTHrP increased the whole cell L-type Ca2+ channel currents and the increase was concentration dependent. rPTHrP, at a concentration of 62.5 nM, increased the L-type Ca2+ channel current by 122+/-25%. bPTH was less potent. A concentration of 7.5 microM bPTH increased the current by 99+/-24%. Results obtained with rPTH were similar to those obtained using bPTH. Single channel measurements, using the cell-attached version of the patch clamp technique, showed an increase in both the number of channel openings and the mean open time when the cells were exposed to rPTHrP. This suggested that rPTHrP affected the gating of L-type Ca2+ channels in UMR 106 cells. This study demonstrates that the actions of bPTH and rPTHrP in UMR cells are mediated in part by extracellular Ca2+ entry. PTHrP, a paracrine agent important in development, is more potent in regulating Ca2+ entry than PTH.
    Life Sciences 01/2002; 70(5):503-15. · 2.56 Impact Factor
  • American Journal of Hypertension 01/2002; 14(12):1273-5. · 3.67 Impact Factor
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    ABSTRACT: The activity of CVT-E002, an aqueous extract containing mainly oligosaccharides and polysaccharides from North American ginseng (Panax quinquefolium), as an immunobooster on murine spleen cells and peritoneal macrophages, was studied in-vitro. CVT-E002 stimulated the proliferation of normal mouse spleen cells, of which the major responding subpopulation was identified as B lymphocytes. CVT-E002 also activated peritoneal exudate macrophages leading to enhanced interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) production. In addition, CVT-E002 stimulated in-vivo immunoglobulin G (IgG) production in treated mice. These results identify some of the immunomodulating activities of CVT-E002 and suggest its use clinically for the modulation of immune responses.
    Journal of Pharmacy and Pharmacology 12/2001; 53(11):1515-23. · 2.03 Impact Factor
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    ABSTRACT: A series of N(1)- and N(2)-propargylphenelzine derivatives and analogues (1-7) was synthesized. In addition to their activity as monoamine oxidase inhibitors, two of the compounds, N(1)- and N(2)-propargylphenelzines (3 and 6), were found to be potent at preventing DSP-4-induced noradrenaline (NA) depletion in mouse hippocampus, suggesting that they have neuroprotective properties.
    Bioorganic & Medicinal Chemistry Letters 11/2001; 11(20):2715-7. · 2.34 Impact Factor
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    ABSTRACT: The ability of N1-propargylphenelzine and related N1-propargylhydrazines to inhibit monoamine oxidase-A (MAO-A) and -B (MAO-B) and to prevent N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4)-induced noradrenergic neurotoxicity was examined. N1-Propargylphenelzine strongly inhibited MAO-A and MAO-B in in vitro assays using rat brain or liver as the enzyme source. In ex vivo studies in rats, both intraperitoneal and oral administration of N1-propargylphenelzine strongly inhibited brain and liver MAO-A and MAO-B. The extent of ex vivo MAO inhibition and increased levels of noradrenaline and 5-hydroxytryptamine by N1-propargylphenelzine was comparable to that of phenelzine. Unlike phenelzine, however, N1-propargylphenelzine did not elevate γ-aminobutryic acid (GABA) concentrations in rat brain. A single intraperitoneal administration of N1-propargylphenelzine to mice, 1 week prior to sacrifice, reduced DSP-4-induced depletion of noradrenaline in the hippocampus. The brains of N1-propargylphenelzine-treated mice from the DSP-4 neurotoxicity experiments had normal MAO-B activity, but MAO-A was significantly inhibited; this was in contrast to animals that had received (–)-deprenyl, who showed normal MAO-A activity but a decrease of MAO-B. The present results indicate that N1-propargylphenelzine may be a useful neuroprotective compound with a long-term in vivo propensity to inhibit MAO-A. Drug Dev. Res. 53:15–21, 2001. © 2001 Wiley-Liss, Inc.
    Drug Development Research 07/2001; 53(1):15 - 21. · 0.87 Impact Factor
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    ABSTRACT: Alcoholic extracts of the roots and leaves of three Echinacea species (E. purpurea, E. angustifolia and E. pallida) were analysed for the presence of characteristic chemicals by HPLC directly coupled to ultraviolet absorbance and electrospray mass spectrometric detectors. The method permitted rapid characterization and tentative identification of a large number of caffeoyl conjugates and alkamides in all the samples investigated. The roots of the three species differed markedly in their contents of characteristic compounds. Cichoric acid and verbascoside predominated in extracts of E. purpurea root whereas cynarine and dodeca-2E,4E,8Z,10Z/E-tetraenoic acid isobutylamide were the major chemicals characteristic of E. angustifolia root extracts. Echinacoside and 6-O-caffeoylechinacoside predominated in extracts of E. pallida roots. Characteristic alkamides were also examined by electrospray tandem mass spectrometry (MS/MS) and these compounds provided characteristic fragmentation patterns. Extracts of the roots and leaves of all three species were found to have antioxidant properties in a free radical scavenging assay and in a lipid peroxidation assay.
    Journal of Pharmacy and Pharmacology 07/2001; 53(6):849-57. · 2.03 Impact Factor
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    ABSTRACT: A combination herbal product containing American ginseng extract, Panax quinquefolium, (200 mg) and Ginkgo biloba extract (50 mg) (AD-FX; CV Technologies, Edmonton, Alta.) was tested for its ability to improve the symptoms of attention-deficit hyperactivity disorder (ADHD). Open study. 36 children ranging in age from 3 to 17 years who fit the diagnostic criteria for ADHD. AD-FX capsules were taken twice a day on an empty stomach for 4 weeks. Patients were instructed not to change any other medications during the study. At the beginning of the study, after 2 weeks, and then at the end of the 4-week trial, parents completed the Conners' Parent Rating Scale--revised, long version, a questionnaire that assesses a broad range of problem behaviours (and was used as an indication of ADHD symptom severity). After 2 weeks of treatment, the proportion of the subjects exhibiting improvement (i.e., decrease in T-score of at least 5 points) ranged from 31% for the anxious-shy attribute to 67% for the psychosomatic attribute. After 4 weeks of treatment, the proportion of subjects exhibiting improvement ranged from 44% for the social problems attribute to 74% for the Conners' ADHD index and the DSM-IV hyperactive-impulsive attribute. Five (14%) of 36 subjects reported adverse events, only 2 of which were considered related to the study medication. These preliminary results suggest AD-FX treatment may improve symptoms of ADHD and should encourage further research on the use of ginseng and Ginkgo biloba extracts to treat ADHD symptoms.
    Journal of psychiatry & neuroscience: JPN 06/2001; 26(3):221-8. · 6.24 Impact Factor
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    ABSTRACT: Under normal resting conditions, little or no nitric oxide synthase (NOS) activity can be measured in vascular smooth muscle cells. However NOS activity may be observed when vascular smooth muscle is exposed to certain stimulants, for example lipopolysaccharide or phenylephrine. The present study was designed to test the hypothesis that under resting conditions vascular smooth muscle NOS activity is under tonic inhibition. The results presented here indicate that under resting conditions, vascular smooth muscle NOS activity may be inhibited by protein kinases.Phenylephrine (PE) was used to induce concentration dependent contractions of endothelium-denuded aortic rings prepared from Sprague-Dawley rats. The rings were suspended in Sawyer-Bartlestone chambers which were filled with Krebs solution. The chambers were maintained at 37C, and gassed with 95% oxygen/5% carbon dioxide. A basal tension of 1.0 g was found to produce optimal contractile responses. Absence of any response to acetylcholine was used as the criterion to ensure adequate removal of the endothelium. Pre-treatment of the rings with H-7, a non-specific inhibitor of protein kinases, attenuated the PE-induced response. N-nitro-L-Arginine (L-NNA) and N-methyl-L-Arginine (L-NMA), both NOS inhibitors, as well as aminoguanidine (AG), a selective inhibitor of inducible NOS, all significantly reduced the H-7-induced inhibition of contraction. The effects of L-NNA, L-NMA and AG were all reversed by L-arginine but not D-arginine. H-89, a selective protein kinase A inhibitor, did not significantly inhibit the PE-induced contraction. However, calphostin C, a specific protein kinase C inhibitor, significantly decreased the PE-induced contraction. Direct measurement of NO with NO-sensitive electrodes showed that H-7 and calphostin C both significantly decreased NO production by PE-stimulated aortic rings. These results indicate that under normal conditions vascular smooth muscle NOS activity is inhibited by the action of protein kinase C but not protein kinase A.
    01/2001;
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    ABSTRACT: To determine the concentrations of chemical characteristic to extracts of leaves and flowers of Hypericum perforatum (St John's wort) in a number of selected samples and, following chemical characterization, to investigate the effects of these extracts on several pharmacological properties including effects of the extracts on inhibition of 5-hydroxytryptamine (5-HT) uptake and on antioxidant properties. The samples were analyzed for the presence of characteristic chemicals by high performance liquid chromatography (HPLC) directly coupled to ultraviolet wavelength absorbance and positive or negative mode electrospray mass spectrometric detection. The effects of extracts on 5-HT uptake were determined by quantifying 3H-5-HT incorporation into rat hippocampal prisms. Estimates of effects of extracts on free radical scavenging capacity were made using a dynamic assay based on the ability of compounds to prevent the initiation of a colored reaction produced by the horseradish peroxidase catalyzed formation of hydroxyl free radicals from hydrogen peroxide using 2',2'-azinobis (3-ethylbenzthiazoline-6-sulfonic acid) as the color indicator. The chemical profile of a number of extracts were determined and found to differ substantially from each other. Inhibition of 5-HT uptake was found to correlate with hyperforin content and free radical scavenging capacity was found to correlate with the content of several flavonoids including quercetin and hyperoside. Standardized extracts of H perforatum varied substantially in the concentration of several characteristic chemicals. The correlation between pharmacological activity and certain characteristic chemicals found in these extracts indicates that the medicinal benefit derived from selected extracts will vary considerably depending on their chemical composition.
    Acta Pharmacologica Sinica 01/2001; 21(12):1145-52. · 2.35 Impact Factor
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    ABSTRACT: -Vascular actions of progesterone have been reported, independently of estrogen, affecting both blood pressure and other aspects of the cardiovascular system. To study possible mechanisms underlying these effects, we examined the effects of P in vivo in intact rats and in vitro in isolated artery and vascular smooth muscle cell preparations. In anesthetized Sprague-Dawley rats, bolus intravenous injections of P (100 µg/kg) significantly decreased pressor responses to norepinephrine (0.3 µg/kg). In vitro, progesterone (10(-8) to 10(-5) mmol/L) produced a significant, dose-dependent relaxation of isolated helical strips, both of rat tail artery precontracted with KCl (60 mmol/L) or arginine vasopressin (3 nmol/L), and of rat aorta precontracted with KCl (60 mmol/L) or norepinephrine (0.1 µmol/L). In isolated vascular smooth muscle cells, progesterone (5x10(-)(7) mol/L) reversibly inhibited KCl (30 mmol/L) -induced elevation of cytosolic-free calcium by 64.1+/-5.5% (P:<0.05), and in whole-cell patch-clamp experiments, progesterone (5x10(-6) mol/L) reversibly and significantly blunted L-type calcium channel inward current, decreasing peak inward current to 65.7+/-4.3% of the control value (P:<0.05). Our results provide evidence that progesterone is a vasoactive hormone, inhibiting agonist-induced vasoconstriction. The data further suggest that progesterone effects on vascular tissue may, at least in part, be mediated by modulation of the L-type calcium channel current activity and, consequently, of cytosolic-free calcium content.
    Hypertension 01/2001; 37(1):142-147. · 6.87 Impact Factor

Publication Stats

2k Citations
721.54 Total Impact Points

Institutions

  • 1986–2005
    • University of Alberta
      • • Department of Physiology
      • • Division of Endocrinology
      Edmonton, Alberta, Canada
    • Jinan University (Guangzhou, China)
      Shengcheng, Guangdong, China
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 1991–2002
    • The University of Hong Kong
      • Department of Biology
      Hong Kong, Hong Kong
  • 2000
    • Queen Mary Hospital
      Hong Kong, Hong Kong
  • 1999
    • National Research Institute of Chinese Medicine
      T’ai-pei, Taipei, Taiwan
  • 1995
    • Università degli studi di Palermo
      • Department of internal medicine and medical specialties (DIMIS)
      Palermo, Sicily, Italy
  • 1994
    • Wayne State University
      • Department of Internal Medicine
      Detroit, MI, United States
  • 1993
    • Yan Shan University
      Shengcheng, Guangdong, China
    • Cornell University
      • Cardiovascular Center
      Ithaca, NY, United States
  • 1989–1993
    • Radboud University Nijmegen
      • Department of Organismal Animal Physiology
      Nymegen, Gelderland, Netherlands
    • Johns Hopkins Medicine
      • Department of Environmental Health Sciences
      Baltimore, MD, United States
  • 1983–1993
    • The Chinese University of Hong Kong
      • Department of Biology
      Hong Kong, Hong Kong
  • 1989–1992
    • Taipei Veterans General Hospital
      T’ai-pei, Taipei, Taiwan
  • 1978–1989
    • Texas Tech University Health Sciences Center
      • Department of Medicine
      El Paso, Texas, United States
    • Universidad de Valparaíso (Chile)
      Ciudad de Valparaíso, Valparaíso, Chile
  • 1987–1988
    • Hospices Civils de Lyon
      Lyons, Rhône-Alpes, France
    • University of Hull
      Kingston upon Hull, England, United Kingdom
  • 1984
    • Toho University
      • Department of Biology
      Edo, Tōkyō, Japan
    • University Medical Center Health System
      Lubbock, Texas, United States
  • 1973–1984
    • Columbia University
      • Department of Pharmacology
      New York City, New York, United States
  • 1975
    • CUNY Graduate Center
      New York City, New York, United States
    • City University of New York - Brooklyn College
      • Department of Biology
      Brooklyn, NY, United States
  • 1967–1974
    • Yale University
      New Haven, Connecticut, United States